Induction of MicroRNA-221 by Platelet-derived Growth Factor Signaling Is Critical for Modulation of Vascular Smooth Muscle Phenotype

被引:275
作者
Davis, Brandi N. [1 ,2 ]
Hilyard, Aaron C. [1 ]
Nguyen, Peter H. [1 ,2 ]
Lagna, Giorgio [1 ]
Hata, Akiko [1 ,2 ]
机构
[1] Tufts Med Ctr, Mol Cardiol Res Inst, Boston, MA 02111 USA
[2] Tufts Univ, Sch Med, Dept Biochem, Boston, MA 02111 USA
基金
美国国家卫生研究院;
关键词
SERUM RESPONSE FACTOR; POSTTRANSCRIPTIONAL REGULATION; PULMONARY-HYPERTENSION; BREAST-CANCER; C-KIT; MYOCARDIN; EXPRESSION; MIR-221; TUMORS; CELLS;
D O I
10.1074/jbc.M808788200
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The platelet-derived growth factor (PDGF) signaling pathway is a critical regulator of animal development and homeostasis. Activation of the PDGF pathway leads to neointimal proliferative responses to artery injury; it promotes a switch of vascular smooth muscle cells (vSMC) to a less contractile phenotype by inhibiting the SMC-specific gene expression and increasing the rate of proliferation and migration. The molecular mechanism for these pleiotropic effects of PDGFs has not been fully described. Here, we identify the microRNA-221 (miR-221), a small noncoding RNA, as a modulator of the phenotypic change of vSMCs in response to PDGF signaling. We demonstrate that miR-221 is transcriptionally induced upon PDGF treatment in primary vSMCs, leading to down-regulation of the targets c-Kit and p27Kip1. Down-regulation of p27Kip1 by miR-221 is critical for PDGF-mediated induction of cell proliferation. Additionally, decreased c-Kit causes inhibition of SMC-specific contractile gene transcription by reducing the expression of Myocardin (Myocd), a potent SMC-specific nuclear coactivator. Our study demonstrates that PDGF signaling, by modulating the expression of miR-221, regulates two critical determinants of the vSMC phenotype; they are SMC gene expression and cell proliferation.
引用
收藏
页码:3728 / 3738
页数:11
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